Skp1, a component of the ubiquitin E3 ligases, was found to be decreased in the brains of sporadic Parkinson's disease (PD) patients, and its overexpression prevented death of murine neurons in culture. Here we expose the neuroprotective role of the Drosophila skp1 homolog, skpA, in the adult brain. Neuronal knockdown of skpA leads to accumulation of ubiquitinated protein aggregates and loss of dopaminergic neurons accompanied by motor dysfunction and reduced lifespan.
View Article and Find Full Text PDFBackground: Protein aggregation in neurons is a prominent pathological mark of neurodegeneration. In Parkinson's disease (PD), inclusions of the α-Synuclein (α-Syn) protein form the Lewy bodies in dopaminergic (DA) neurons. Ectopic expression of human α-Syn inDrosophila neurons leads to the protein accumulation, degeneration of DA neurons and locomotor deterioration, and therefore constitutes the present fly PD model.
View Article and Find Full Text PDFIn this Article originally published, owing to a technical error, the author 'Laurent Chirio' was mistakenly designated as a corresponding author in the HTML version, the PDF was correct. This error has now been corrected in the HTML version. Further, in Supplementary Table 3, the authors misspelt the surname of 'Danny Meirte'; this file has now been replaced.
View Article and Find Full Text PDF